Proliferation of resident glomerular cells and the accumulation of mesangial matrix are histologic abnormalities which are observed in the course of many progressive glomerular diseases. We explored the potential regulatory effects of transforming growth factor-B (TGF-B) on these processes. We found that cultured mouse glomerular endothelial, mesangial, and epithelial cells as well as isolated rat glomeruli possess high affinity receptors for TGF-B. We also found that while TGF-B consistently inhibited the proliferation of glomerular endothelial and epithelial cells it acted as a bifunctional regulator of mesangial cell proliferation. The presence of TGF-B receptors on each glomerular cell type and on isolated glomeruli, the multiple potential sources of TGF-B within the glomerulus and the demonstrated responsiveness of cultured glomerular cells to TGF-B combine to suggest that potentially important interactions may occur between resident glomerular cells and TGF-B in vivo.